Microbiology Virus Structure & Function Quiz

Viruses are acellular microbes, meaning they lack the cellular structure found in bacteria, fungi, and protozoa. They do not have organelles, membranes, or metabolic systems of their own. Instead, they consist of genetic material packaged within a protein coat. Because they cannot conduct independent life processes, they are not classified as organisms. Their simplicity and dependency on host cells distinguish them from all other biological life forms.

Viruses do not replicate independently; they must enter a host cell and use that cell’s enzymes, ribosomes, and energy sources. This intracellular dependency defines them as obligate intracellular parasites. They cannot divide, metabolize, or synthesize molecules outside a living cell. Replication requires hijacking the host’s biochemical machinery to produce viral components, assemble new particles, and complete their replication cycle.

Viruses have no metabolic processes of their own. They lack enzymes, ribosomes, and pathways required for energy production or biosynthesis. Instead, they commandeer host cell pathways and redirect them toward producing viral RNA/DNA and proteins. This hijacking completely replaces normal host metabolic output with viral products, allowing new virions to form. Their lack of metabolism is a central reason they are not considered living organisms.

Viruses do not fall within a single taxonomic group because they do not meet criteria for cellular life. They show extreme diversity in structure, genome type, replication strategies, and host range. This diversity surpasses that of cellular organisms, spanning DNA viruses, RNA viruses, retroviruses, bacteriophages, and giant viruses. They infect every known category of life, including bacteria, archaea, plants, fungi, and animals.

Viruses are the most numerous biological entities on Earth, far exceeding bacteria and eukaryotes. Oceans, soil, and the human microbiome contain astronomically large virus populations. For example, a teaspoon of seawater can contain millions of viral particles. Their abundance contributes significantly to gene transfer, ecological cycling, microbial population control, and global biodiversity.

Virology is a specialized scientific discipline dedicated to studying viruses, rather than grouping them with cellular microbes. Because viruses differ fundamentally from living organisms, they require unique approaches to classification, experimentation, taxonomy, and treatment. Virology examines viral structure, replication, pathogenicity, and evolution, separating them from traditional branches of microbiology.

Viruses are drastically smaller than bacterial and eukaryotic cells, often by several orders of magnitude. Many viruses range from 20–300 nm, while bacteria are typically 1–10 µm. This small size enables rapid entry into host cells, evasion of immune detection, and high-density replication. Their size is a distinguishing structural feature.

All viruses contain a genome—either DNA or RNA, single or double-stranded—encased in a protective protein shell called the capsid. This minimal structure allows efficient packaging, protection, and delivery of genetic material into host cells. Other structures such as envelopes are optional and host-derived, but the genome–capsid combination is universal to viruses.

Viruses exhibit wide structural diversity, forming helical rods, polyhedral shapes, or complex bacteriophage structures. These shapes help determine mechanisms of infection, stability, and host recognition. They do not exhibit colors, sounds, or sensory characteristics—these options are biological metaphors, not structural features.

Many pathogens listed—such as Salmonella (bacterium) and malaria (protozoan)—are not viruses. True viral examples include polio, papilloma virus, measles, cowpox, smallpox, Ebola, and West Nile virus. These pathogens share the defining viral traits of acellularity and dependency on host cell machinery.

Viral capsids typically take one of three shapes: helical, polyhedral (often icosahedral), or complex (such as bacteriophages with heads and tails). These structural patterns are determined by the arrangement of capsid proteins and influence viral stability and host-cell entry mechanisms.

Viruses may be enveloped or nonenveloped. Enveloped viruses possess a host-derived phospholipid bilayer that aids entry and immune evasion, while nonenveloped viruses lack this layer and typically exit the cell by lysis. This distinction strongly affects transmission, environmental stability, and pathogenicity.

Lytic replication involves entry of viral genetic material into the host cell, replication using host enzymes, expression of viral proteins, assembly of new virions, and release through lysis. This release destroys the host cell, generating many new infectious particles. The lytic cycle contrasts with lysogeny, which does not immediately kill the cell.

Enveloped viruses exit by budding from the host membrane, acquiring a lipid envelope. Nonenveloped viruses accumulate within the cell and are released by bursting (lysis), which kills the host. These are the two major mechanisms of viral release and determine the virus’s environmental stability and infection strategy.

Lysogeny involves the integration of viral DNA into the host genome, forming a prophage or provirus. This allows dormant persistence across many cell generations. As the cell divides, the viral genome is replicated along with the host’s DNA, enabling long-term maintenance without lysis. Environmental triggers may later reactivate the virus into the lytic cycle.

Viruses significantly impact evolution because they transfer genes horizontally between organisms, altering genetic diversity. They also cause a vast range of diseases, influencing natural selection. Their roles in gene transfer, recombination, and co-evolution make them major evolutionary drivers.

Retroviruses carry RNA genomes and use reverse transcriptase to convert RNA into DNA inside a host. This DNA integrates into the host genome, enabling persistent infection. HIV is the best-known retrovirus. This reverse flow of genetic information distinguishes retroviruses from DNA viruses and most RNA viruses.

HIV parasitizes human T cells, specifically CD4+ helper T cells. The virus replicates inside these immune cells, leading to cell death and profound immune weakness. This weakened immune system results in vulnerability to many microorganisms, including bacteria, fungi, protozoa, and opportunistic pathogens.

Historically, viruses were viewed as small, simple entities, likely derived from rogue genetic material (“renegade genes”), and closely related to their hosts. Because they lack cellular structure, they were thought to be simpler than bacteria and incapable of independent life. These ideas shaped early virology.

The discovery of Mimivirus challenged long-standing assumptions about viruses. Mimivirus is larger than some bacteria, has both DNA and RNA processing genes, and carries over 1,000 genes—far more than typical viruses. Its size and complexity blur the boundary between viruses and cellular life.

Viroids are infectious plant agents consisting solely of short circular RNA strands with high internal complementary base pairing. They contain no protein coat and do not encode proteins. Their simplicity makes them the smallest known infectious particles.

Viroids are believed to cause disease through RNA silencing, a mechanism where the viroid RNA interferes with plant mRNAs. This disrupts gene expression, leading to developmental abnormalities and disease symptoms. Unlike viruses, viroids do not rely on protein synthesis or capsid formation.